| First Author | Mojica C | Year | 2018 |
| Journal | Neuropharmacology | Volume | 135 |
| Pages | 529-535 | PubMed ID | 29677582 |
| Mgi Jnum | J:305080 | Mgi Id | MGI:6510190 |
| Doi | 10.1016/j.neuropharm.2018.04.010 | Citation | Mojica C, et al. (2018) Maternal nicotine exposure effects on adolescent learning and memory are abolished in alpha(alpha)2* nicotinic acetylcholine receptor-null mutant mice. Neuropharmacology 135:529-535 |
| abstractText | The objective of the current study is to test the hypothesis that the deletion of alpha(alpha)2* nicotinic acetylcholine receptors (nAChRs) (encoded by the Chrna2 gene) ablate maternal nicotine-induced learning and memory deficits in adolescent mice. We use a pre-exposure-dependent contextual fear conditioning behavioral paradigm that is highly hippocampus-dependent. Adolescent wild type and alpha2-null mutant offspring are exposed to vehicle or maternal nicotine exposure (200 mug/ml, expressed as base) in the drinking water throughout pregnancy until weaning. Adolescent male offspring mice are tested for alterations in growth and development characteristics as well as modifications in locomotion, anxiety, shock-reactivity and learning and memory. As expected, maternal nicotine exposure has no effects on pup number, weight gain and only modestly reduces fluid intake by 19%. Behaviorally, maternal nicotine exposure impedes extinction learning in adolescent wild type mice, a consequence that is abolished in alpha2-null mutant mice. The effects on learning and memory are not confounded by alternations in stereotypy, locomotion, anxiety or sensory shock reactivity. Overall, the findings highlight that the deletion of alpha2* nAChRs eliminate the effects of maternal nicotine exposure on learning and memory in adolescent mice. |
